Origination Vs Preparation

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The source of the Sars-Cov-2 virus[1] has to date been suggested to have either ‘spilled’ over from wildlife to humans, i.e bat to human transmission (zoonotic)[2], or to have emerged, without direct animal transfer from a virology research lab in Wuhan China. Other proposals of origination have yet to make their way into collective consciousness, but no doubt there are some lurking at the edge of plausibility! The research community already accepts that ‘natural spillovers’ occur, these have been recorded for many decades, and highlighted in books and journals that they can cause dangerous and transmissible outbreaks, so scientists do not need any further proof for this proposal.

Obviously, the project to identify the source of the coronavirus pandemic has moral, legal, and political significance; but with regard to global public health, individual response and to the crucial project of pandemic-proofing ourselves for the future, it is probably fair to state that its outcome matters only at the margins. More importantly is the recognition that we are all more connected to one another than we ever imagined.

Of course, we may never know exactly how the coronavirus that causes Covid-19 spread to humans. Scientists still have not pinpointed the origin of the influenza strain that killed millions[3] in 1918. Although Civet cats were speculated within months to be the intermediate host in a 2003 SARS outbreak, it took 14 years to confirm it.[4] It was not until 2017 that that virus was finally traced back to bats. The lab that solved the mystery? The Wuhan Institute of Virology.[5]

As set out on the Massive Science blog – If the question is “are both hypotheses possible?” for the origination of SARS-Cov-2 the answer is yes. Both are possible. If the question is “are they equally likely?” the answer is absolutely not. One hypothesis requires a colossal cover-up and the silent, unswerving, leak-proof compliance of a vast network of scientists, civilians, and government officials for over a year. The other requires only for biology to behave as it always has, for a family of viruses that have done this before to do it again. The zoonotic spillover hypothesis is simple and explains everything. It is scientific malpractice to pretend that one idea is equally as meritorious as the other.[6]

What to Focus on.

Instead of just calling for a new and better inquiry into origins and potentially creating serious racial and geopolitical ructions (albeit this pleading is likely to fail), let us instead stipulate that pandemics of the type we have all been managing can result from natural spillovers or from laboratory accidents and then instead move along to larger health implications of risk.

The risk of adverse outcomes in infectious disease are underpinned and magnified by changes in metabolic function and quality – in effect the greater the deviation from metabolic optimal status, the greater the likelihood of death once infected. Whilst we would all like to believe that natural immunity once optimised would be 100% effective in infection protection, there are many variables that will influence this resilience. Whilst some of these are known and understood others are either unknown or are in early stages of discovery.

Lifestyle medicine and functional medicine include numerous intersecting approaches to human health management, rather than isolated targets, and as such require engagement, buy in and patterns of behaviour change to become embedded. From food production, environmental pressures, social engagement, poverty alleviation and nutrient consumption, there are numerous internal and external challenges. This means that collective action, from business, consumers, and politicians as well as health care professionals is needed.

Air Pollution

One area that is finally attracting serious attention is air quality and the related impact on lung function especially asthma in children[7] and other organ related damage. Particulates found in air from various sources are like viruses, mostly very small ultrafine chemicals. Childhood asthma remains a global epidemic that is likely to grow with the anticipated rise in particulate air pollution exposures due to the effects of climate change.[8]

New research, published in the American Journal of Respiratory and Critical Care Medicine,[9] followed almost 400 mothers and their children through pregnancy and afterwards in Boston, US. The level of ultra-fine particulates, which are those smaller than 0.1 micrometre, ranged from about 10,000 to 40,000 per cubic centimetres of air. The researchers found that children whose mothers had been exposed to levels of 30,000/cm3 during pregnancy were approximately four times more likely to develop asthma than those whose mothers had been exposed to levels of 15,000/cm3. This difference in pollution is roughly the change seen when going from a backstreet to a busy road. As well as trying to avoid polluted places, Wright, a respiratory physician, and lead author tells her patients to consider taking antioxidants, as these have been shown to reduce inflammation caused by particle pollution.

Air pollution impacted Sars Cov-2 outcomes[10] and also appears linked to one of most rapidly growing metabolic dysfunctions namely diabetes, as well as reduced Vitamin D synthesis. A common thread in patterns of risk related to infectious disease outcomes.

Experimental studies conducted for other respiratory viruses support the hypothesis that air pollution exposure may facilitate the occurrence of Covid-19 infection through a decrease in immune response. In vitro, animal and human studies have also reported that exposure to air pollutants leads to increased mucosal permeability and oxidative stress, decreased antioxidants and surfactant antimicrobial proteins, as well as impaired macrophage phagocytosis. In addition, SARS-Cov-2 entry in host cells through ACE 2 requires the cleavage of the viral spike protein by proteases, and such protease activity may be increased by air pollution, as is documented for several other respiratory viruses.

Supply and Demand

Attractive though it may be to focus on virus origination, and useful in terms of future planning, the more pressing challenge is that our current lifestyles propagate risk via immune suppression, disorganisation and reduced capacity for resilience. Whilst some of the nuances may be lost on many of the politicians, and even on the medical professions, the direct cost of managing the unintended consequences is leading to a rapid loss in the UK and elsewhere of primary care physicians[11] at a faster rate than renewal.

There is clearly a mismatch between demand (people slowly migrating into chronic disease) and supply (health care providers). There needs to be a focus on public health policies to drive the narrative, that social and personal health care is essential to prevent economic, and societal disintegration because of a constellation of changing climate, changing health dynamics such as diabetes expansion[12] which has doubled to almost 5m in the UK in last 20 years and is one of the top 10 causes of death globally. Together with cardiovascular disease, cancer and respiratory disease, these conditions account for over 80% of all premature non-communicable diseases (NCDs) deaths and make people far more susceptible to infectious disease. Diabetes alone ensures the second biggest negative total effect[13] on reducing global health adjusted life expectancy worldwide.

Considering the nature of these underlying conditions such as obesity diabetes, pollution, inflammation and hypertension, lifestyle-based approaches[14] driven by central government’s actions to change food choice behaviour are likely to be one of our best tools in order to address ongoing and future disease burden during pandemics. Post Covid-19 related changes in health status indicated that one in five people have a new disability after hospitalisation and one in ten have ongoing symptoms 12 weeks after a positive test, with the impact far greater in young people.[15],[16] One more positive finding is that most people infected with SARS-Cov-2 will probably make antibodies against the virus for most of their lives, albeit their efficacy may be blunted by variants.[17]


Regardless of whether the exact underlying mechanisms are currently understood, the tenets of lifestyle medicine have extraordinary power to improve the health of the population, both overall as well as in the face of unknown future pandemics. For instance, a wide variety of dietary approaches have been shown to be effective in providing long-term weight loss, reductions in blood pressure,[18] improved glycaemic control,[19] and even reversal of type 2 diabetes.[20] These include the dietary approaches to stop hypertension (DASH) and the traditional Mediterranean diets and use of food supplements, vitamins and minerals.[21]

The primary interface between the external world and us is found at the mucosal surfaces, where we share our wet tissues with a vast population of organisms, that are not us. With the increasing ability to understand microbial metabolic and functional capabilities, the microbiome’s contribution to human health and various diseases is becoming more evident.[22] Disruption of gut microbiota as related to modern lifestyles increases susceptibility to infection and sepsis through several mechanisms, including.

(a) allowing for the expansion of pathogenic intestinal bacteria,

(b) priming the immune system for a robust pro-inflammatory response, and

(c) decreasing production of beneficial microbial products such as short-chain fatty acids.

If there is disruption at the level of barrier immunity, there will be loss of immune homeostasis with an associated risk of immune or inflammatory disorders. All hall marks of adverse immune responses to infection. Further qualifying that microbiota modulation via diet and lifestyle should be considered as a target for personalised nutrition and therapy.

Specific nutrients and live microbes can therefore be considered strategic bioactives for the maintenance, preservation, or restoration of host–microbe symbiosis. A major way of leveraging prevention and recovery in chronic diseases and iatrogenic conditions is intimately related to the management and the monitoring of intestinal ecology, which can be achieved through diet and lifestyle interventions.[23] The western diet high in fat and sugar has many short and long term consequences, and increasingly scientists are understanding what nutritional therapists have recognised for decades, it damages the health of the gut and related outcomes are always detrimental to health, resilience and vitality.[24]


[1] Bloom JD, Chan YA, Baric RS, Bjorkman PJ, Cobey S, Deverman BE, Fisman DN, Gupta R, Iwasaki A, Lipsitch M, Medzhitov R, Neher RA, Nielsen R, Patterson N, Stearns T, van Nimwegen E, Worobey M, Relman DA. Investigate the origins of COVID-19. Science. 2021 May 14;372(6543):694

[2] Dhama K, Patel SK, Sharun K, et al. SARS-CoV-2 jumping the species barrier: Zoonotic lessons from SARS, MERS and recent advances to combat this pandemic virus. Travel Med Infect Dis. 2020; 37:101830.

[3] Hoag H. Study revives bird origin for 1918 flu pandemic. Nature Feb 16 2014

[4] Reuters Health Care and Pharma accessed on line 28.5.2021 China scientists say SARS-civet cat link proved.

[5] Cyranoski D. Bat cave solves mystery of deadly SARS virus – and suggests new outbreak could occur. Nature New 1 December 2017

[6] Samorodnitsky D. The lab-leak hypothesis for COVID-19 is becoming a conspiracy theory. To explain where SARS-CoV-2 came from, look at processes with scientific explanations and precedents. Reviewed 1.6.21

[7] Lavigne E, Donelle J, Hatzopoulou M, Van Ryswyk K, van Donkelaar A, Martin RV, Chen H, Stieb DM, Gasparrini A, Crighton E, Yasseen AS 3rd, Burnett RT, Walker M, Weichenthal S. Spatiotemporal Variations in Ambient Ultrafine Particles and the Incidence of Childhood Asthma. Am J Respir Crit Care Med. 2019 Jun 15;199(12):1487-1495.

[8] Yang J, Zhao Y, Cao J, Nielsen CP. Co-benefits of carbon and pollution control policies on air quality and health till 2030 in China. Environ Int. 2021 Jul; 152:106482. doi: 10.1016/j.envint.2021.106482. Epub 2021 Mar 9.

[9] Wright RJ, Hsu HL, Chiu YM, Coull BA, Simon MC, Hudda N, Schwartz J, Kloog I, Durant JL. Prenatal Ambient Ultrafine Particle Exposure and Childhood Asthma in the Northeastern United States. Am J Respir Crit Care Med. 2021 May 21. doi: 10.1164/rccm.202010-3743OC.

[10] Bourdrel T, Annesi-Maesano I, Alahmad B, Maesano CN, Bind MA. The impact of outdoor air pollution on COVID-19: a review of evidence from in vitro, animal, and human studies. Eur Respir Rev. 2021 Feb 9;30(159):200242. doi: 10.1183/16000617.0242-2020. PMID: 33568525; PMCID: PMC7879496.

[11] Hodes S, Hussain S, Jha N, Toberty L, Welch E. If general practice fails, The NHS fails. The BMJ opinion 14, May 2021

[12] Diabetes UK accessed online 28.5.2021.

[13] Chen H, Chen G, Zheng X, Guo Y. Contribution of specific diseases and injuries to changes in health adjusted life expectancy in 187 countries from 1990 to 2013: retrospective observational study. BMJ 2019;364: l969

[14] Wood, T.R. and Jóhannsson, G.F. (2020), Metabolic health and lifestyle medicine should be a cornerstone of future pandemic preparedness. Lifestyle Med., 1: e2

[15]  Physical, cognitive and mental health impacts of COVID-19 following hospitalisation – a multi-centre prospective cohort study

PHOSP-COVID Collaborative Group, Christopher E Brightling et al medRxiv 2021.03.22.21254057

[16] Al-Aly, Z., Xie, Y. & Bowe, B. High-dimensional characterization of post-acute sequelae of COVID-19. Nature (2021).

[17] Turner, J.S., Kim, W., Kalaidina, E. et al. SARS-CoV-2 infection induces long-lived bone marrow plasma cells in humans. Nature (2021).

[18] Siervo M, Lara J, Chowdhury S, Ashor A, Oggioni C, Mathers JC. Effects of the Dietary Approach to Stop Hypertension (DASH) diet on cardiovascular risk factors: a systematic review and meta-analysis. Br J Nutr. 2015 Jan 14;113(1):1-15. doi: 10.1017/S0007114514003341. Epub 2014 Nov 28.

[19] Becerra-Tomás N, Blanco Mejía S, Viguiliouk E, Khan T, Kendall CWC, Kahleova H, Rahelić D, Sievenpiper JL, Salas-Salvadó J. Mediterranean diet, cardiovascular disease and mortality in diabetes: A systematic review and meta-analysis of prospective cohort studies and randomized clinical trials. Crit Rev Food Sci Nutr. 2020;60(7):1207-1227. doi: 10.1080/10408398.2019.1565281.

[20] Taylor R. Calorie restriction for long-term remission of type 2 diabetes [published correction appears in Clin Med (Lond). 2019 Mar;19(2):192]. Clin Med (Lond). 2019;19(1):37-42. doi:10.7861/clinmedicine.19-1-37

[21] Samad N, Dutta S, Sodunke TE, Fairuz A, Sapkota A, Miftah ZF, Jahan I, Sharma P, Abubakar AR, Rowaiye AB, Oli AN, Charan J, Islam S, Haque M. Fat-Soluble Vitamins and the Current Global Pandemic of COVID-19: Evidence-Based Efficacy from Literature Review. J Inflamm Res. 2021; 14:2091-2110

[22] Malard, F., Dore, J., Gaugler, B. et al. Introduction to host microbiome symbiosis in health and disease. Mucosal Immunol 14, 547–554 (2021)

[23] Bajinka, O., Tan, Y., Abdelhalim, K.A. et al. Extrinsic factors influencing gut microbes, the immediate consequences and restoring eubiosis. AMB Expr 10, 130 (2020).

[24] Ta-Chiang Liu, Justin T. Kern, Umang Jain, Naomi M. Sonnek, Shanshan Xiong, Katherine F. Simpson, Kelli L. VanDussen, Emma S. Winkler, Talin Haritunians, Atika Malique, Qiuhe Lu, Yo Sasaki, Chad Storer, Michael S. Diamond, Richard D. Head, Dermot P.B. McGovern, Thaddeus S. Stappenbeck, Western diet induces Paneth cell defects through microbiome alterations and farnesoid X receptor and type I interferon activation, Cell Host & Microbe, 2021

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